Amygdaloid atrophy in frontotemporal dementia and Alzheimer's disease

• Published in: Neuroscience letters Vol. 335; no. 2; pp. 139 - 143
• Main Authors: Boccardi, M., Pennanen, C., Laakso, M.P., Testa, C., Geroldi, C., Soininen, H., Frisoni, G.B.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 25.12.2002; Elsevier
• Subjects: Aged; Alzheimer; Alzheimer Disease - pathology; Amygdala; Amygdala - pathology; Atrophy; Biological and medical sciences; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dementia; Dementia - pathology; Female; Frontotemporal dementia; Humans; Image Processing, Computer-Assisted; Imaging; Magnetic resonance; Magnetic Resonance Imaging - methods; Male; Medical sciences; Middle Aged; Morphology; Neurology; Statistics, Nonparametric; Amygdala; Imaging; Morphology; Magnetic resonance; Frontotemporal dementia; Alzheimer; Dementia; Human; Nervous system diseases; Alzheimer disease; Central nervous system; Basal ganglion; Nuclear magnetic resonance imaging; Cerebral disorder; Atrophy; Central nervous system disease; Degenerative disease; Brain (vertebrata)
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(02)01169-2

Crude and corrected amygdaloid volumes were computed from magnetic resonance scans in ten patients with frontotemporal dementia (FTD), 25 patients with Alzheimer's disease (AD) and 27 controls. Amygdaloid atrophy was present in FTD ( P<0.005) compared to controls, and a trend for increasing atrophy from controls, through FTD to AD ( P for trend <0.00005) showed that FTD amygdaloid volumes were intermediate between controls and AD. Behavioral and Klüver–Bucy-like symptoms, characteristic of FTD, cannot be explained by amygdaloid atrophy alone.